Journal article
Validating the RedMIT/GFP-LC3 mouse model by studying mitophagy in autosomal dominant optic atrophy due to the OPA1Q285STOP mutation
- Abstract:
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Background
Autosomal dominant optic atrophy (ADOA) is usually caused by mutations in the essential gene, OPA1. This encodes a ubiquitous protein involved in mitochondrial dynamics, hence tissue specificity is not understood. Dysregulated mitophagy (mitochondria recycling) is implicated in ADOA, being increased in OPA1 patient fibroblasts. Furthermore, autophagy may be increased in retinal ganglion cells (RGCs) of the OPA1Q285STOP mouse model.
Aims
We developed a m...
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- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Version of record, pdf, 3.2MB)
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- Publisher copy:
- 10.3389/fcell.2018.00103
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Authors
Funding
Angus Memorial Mitochondrial Fund
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Bibliographic Details
- Publisher:
- Frontiers Media Publisher's website
- Journal:
- Frontiers in Cell and Developmental Biology Journal website
- Volume:
- 6
- Issue:
- SEP
- Pages:
- 103
- Publication date:
- 2018-09-19
- Acceptance date:
- 2018-08-13
- DOI:
- EISSN:
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2296-634X
- Pmid:
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30283778
- Source identifiers:
-
923640
Item Description
- Language:
- English
- Keywords:
- Pubs id:
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pubs:923640
- UUID:
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uuid:6c9e1121-02b2-42e2-a206-2ccd3ef3f0d1
- Local pid:
- pubs:923640
- Deposit date:
- 2018-10-25
Terms of use
- Copyright holder:
- Diot et al
- Copyright date:
- 2018
- Notes:
- Copyright © 2018 Diot, Agnew, Sanderson, Liao, Carver, Neves, Gupta, Guo,Waters, Seto, Daniels, Dombi, Lodge,Morten,Williams, Enver, Iborra, Votruba and Poulton. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
- Licence:
- CC Attribution (CC BY)
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